The proposed research will test the hypothesis that airway obstruction in bilateral recurrent laryngeal nerve paralysis is due to reflex stimulation of the cricothyroid muscle, and that suppression of this reflex would significantly improve the airway, while preserving voluntary cricothyroid contraction during phonation. Previous studies indicate that the cricothyroid is an accessory muscle of respiration and that inspiratory cricothyroid contraction is strongly stimulated by airway obstruction and hypercapnia. Studies by others authors have shown that electrical stimulation of the cricothyroid in the absence of abduction by the posterior cricoarytenoid leads to narrowing of the glottis. It is not known whether physiologic contraction of the cricothyroid has the same effect. The research protocol for the first two years of the grant will test the following hypotheses: 1) Physiologic cricothyroid contraction significantly affects laryngeal resistance; 2) Reflex cricothyroid contraction determines vocal fold position following recurrent laryngeal nerve paralysis; 3) Chemoreceptor input strongly modulates cricothyroid response to airway obstruction; 4) Cricothyroid reflexes can be demonstrated in humans; 5) Voluntary cricothyroid contraction during phonation is unimpaired by respiratory stimuli. Laryngeal resistance and cricothyroid and posterior cricoarytenoid EMG activity will be measured in anesthetized dogs under varying breathing conditions, before and after cod blockade of the recurrent laryngeal nerves. Glottic area will be documented by a video recording of the larynx. Experiments in human subjects will measure EMG activity of the cricothyroid and posterior cricoarytenoid under varying conditions during breathing and phonation. Research in the last three years of the grant period will investigate the changes in vocal fold position and cricothyroid muscle activity over time following recurrent laryngeal nerve paralysis.